Clement A, Henrion-Caude A, Besnard V, Corroyer S
Department of Pediatric Pulmonology, INSERM U515, Hôpital Armand Trousseau, Paris, France.
Am J Respir Crit Care Med. 2001 Nov 15;164(10 Pt 2):S81-4. doi: 10.1164/ajrccm.164.supplement_2.2106069.
Oxidants are involved in a large variety of pulmonary diseases. Among the various cell types that compose the respiratory system, the epithelial cells appear to be a major target for oxidative stress. When cells are exposed to DNA-damaging agents such as oxidants, a feedback control is activated that acts as a brake on the cell cycle to inhibit entry into the S phase until DNA repair is completed. Progression through the G1 phase and the G1-S transition involves sequential assembly and activation of key regulators of the cell cycle machinery, the cyclin-dependent kinases (CDKs). Activity of the CDKs is regulated by several mechanisms, which include the CDK inhibitors (CKIs). The CKI p21(CIP1) appears to play an important role in the response of epithelial cells to oxidants.
氧化剂参与多种肺部疾病。在构成呼吸系统的各种细胞类型中，上皮细胞似乎是氧化应激的主要靶点。当细胞暴露于诸如氧化剂等DNA损伤剂时，一种反馈控制被激活，它就像细胞周期的刹车，抑制进入S期，直到DNA修复完成。通过G1期和G1-S转换的进程涉及细胞周期机制关键调节因子——细胞周期蛋白依赖性激酶（CDK）的顺序组装和激活。CDK的活性受多种机制调节，其中包括CDK抑制剂（CKI）。CKI p21（CIP1）似乎在上皮细胞对氧化剂的反应中起重要作用。
